1. Field of the Invention
The present invention relates generally to implantable cardiac stimulators, such as artificial pacemakers, cardioverters and defibrillators; and more particularly to fixation mechanisms for the lead/electrode assemblies of implantable cardiac stimulators.
2. Discussion of Prior Art
The sinoatrial (S-A) node of the human heart acts as the natural pacemaker by which rhythmic electrical excitation is developed and propagated to the atria, whereupon the atrial chambers contract, pumping blood into the ventricles. The rhythmic excitation is further propagated through the atrioventricular (A-V) node, which imposes a delay, and then via the conduction system consisting of the bundle of His and the Purkinge fibers to the ventricular myocardium, producing contraction of the ventricles. As a result, the oxygen-depleted blood in the right ventricle is pumped through the pulmonary artery to the lungs, and the oxygenated blood in the left ventricle is pumped through the arteries to the body. The right atrium receives the oxygen-depleted blood from the body via the veins, and the left atrium receives oxygenated blood from the lungs.
The actions repeat in a rhythmic cardiac cycle in which the atrial and ventricular chambers alternately contract and pump, relax and fill. One way valves along the veins, between the chambers in the right side and the left side of the heart, and at the exits of the right ventricle and left ventricle prevent backflow of the blood as it moves through the heart and circulatory system.
The S-A node is spontaneously rhythmic, and with a normal excitation and propagation system the heart beats in an organized manner at a regular rate termed sinus rhythm. Disruption of the natural pacing and propagation system as a result of aging or disease is commonly treated by artificial cardiac pacing, in which a cardiac pacemaker is implanted to maintain the desired heart rate.
Implantable artificial cardiac pacemakers, or, more simply, "pacemakers," generally employ a stimulus generator commonly termed a "pulse generator" housed in a case and powered by a self-contained battery, and a lead assembly typically referred to simply as a "lead" having one or more electrodes for conductive coupling to the generator circuitry via a connector integral with the case. The pacing electrode is variously referred to as the stimulating cathodic electrode, the stimulating electrode, or merely the cathode, and the indifferent electrode is alternatively referred to as the reference electrode, the anodic electrode, or simply the anode. The pulse generator and the lead are manufactured and distributed as separate items, the leads being interchangeable with pulse generators of the various types.
Typically, the lead is inserted through the superior vena cava (the great vein which transports unoxygenated blood from the upper part of the body to the right atrium) until the stimulating electrode at the distal end of the lead is brought into proper position within the desired chamber in the right side of the patient's heart. Because it is adapted for intravenous insertion, the lead is sometimes referred to as a "catheter lead"; and because the electrode is adapted to be positioned within the heart, it is often called an "endocardial electrode". The proximal end of the lead is inserted and fastened into the integral connector of the pulse generator case, which is implanted in a subcutaneous pouch formed by an incision in the patient's chest. With dual chamber pacemakers, both chambers of the heart may be stimulated and/or sensed using two separate leads, one of which is introduced into the right atrium and the other into the right ventricle.
By appropriately manipulating the lead, the implanting physician positions and, if necessary, repositions the stimulating electrode to assure consistent "capture" of the heart, that is to say, that the patient's heart responds to each stimulus generated by the pacemaker. In essence, the stimulating electrode serves to impress an electric field, resulting from electrical discharge by the pulse generator, on excitable myocardial tissue in the vicinity of that electrode. This is accomplished via an electrical circuit consisting of the pulse generator, the conducting lead, the stimulating electrode, the indifferent electrode, and the volume conductor comprising the patient's body tissue and fluid.
The pacemaker may be arranged for unipolar or bipolar stimulation according to the configuration and location of the indifferent electrode. For unipolar stimulation, the anode is somewhat remote from the heart, typically constituting part of the metal case that houses the pulse generator. For bipolar pacing, the lead to be implanted is configured with the cathode and the anode insulatively separated from but in close proximity to one another at the distal end of the lead. Typically the cathode is located at or near the tip of the lead and the anode is configured as a ring electrode spaced back one half inch or so from the cathode. Each electrode is connected to its own electrically conductive coil within the lead.
The stimulating electric field generated by the pacemaker in the vicinity of the cathode must be of sufficient impulse strength to initiate a so-called "action potential" and depolarization of cells within the excitable tissue, in order to cause and propagate cardiac stimulation. The smallest electrical impulse necessary to initiate such stimulation is referred to as the "stimulation threshold," or simply the "threshold". In practice, the cardiologist or surgeon will set the stimulation level to comfortably exceed the threshold for the particular patient and pacing system. Indeed, since there is invariably an acute but gradual rise in threshold over a period of from about one to four weeks after the pacemaker is implanted, it is customary to set the stimulus level initially at about four times that of the threshold measured at implant. The increase in acute threshold is attributable in part to the growth of a fibrotic layer of non-excitable tissue of uneven thickness about the electrode tip in contact with the myocardium, which effectively increases the surface area of the electrode and lowers the current density. Another factor is the inflammation reaction at the tip. The chronic threshold is usually observed about four to eight weeks after implantation.
It is common practice to seek to position the stimulating cathodic electrode at the time of implant at a location within the chamber to be paced which offers the lowest threshold and the greatest mechanical stability. Until the stimulating electrode becomes secured in place as a result of fibrotic growth, a period which depends in large measure on the structure and composition of the electrode, it is subject to dislodgement because of the rhythmic contraction and relaxation of the heart, or merely as a consequence of general body movements of the patient.
Various electrode fixation mechanisms have been devised since the inception of the artificial pacemaker to secure the lead (and more particularly, the electrode) in place after positioning by the cardiologist or surgeon. Such mechanisms fall into two categories. Some offer passive fixation, by means of non-invasive devices such as pliant barbs (so-called "tines") attached at or near the lead tip to engage the trabeculae within the heart chamber. Others provide more positive fixation termed "active fixation," of the electrode. The known active fixation mechanisms include corkscrews, hooks, piercing barbs, or other anchoring means arranged at or near the lead tip for penetration of the endocardium upon manipulation of the lead and/or a stylet traversing the lead, following proper positioning of the cathode.
The principal disadvantages of active fixation mechanisms are that (1) they are quite difficult to manufacture, and are therefore very costly, because of the relatively small size of the lead and the necessarily tiny size of the functioning parts of the mechanism which must be attached to the distal end of the lead; (2) they require penetration of the tissue which can cause trauma, particularly if the lead must be unhooked for repositioning of the electrode and re-affixed to the tissue at a more desirable location for lower threshold capture, or if the lead must be withdrawn; and (3) they can make the lead extremely difficult to implant unless the surgeon is highly accomplished in the techniques of inserting, positioning, manipulating and affixing a lead with that particular mechanism by having performed the procedure numerous times. With respect to the latter disadvantage, it is recognized that implanting surgeons tend to develop a "feel" for leads having particular fixation mechanisms, and express a certain comfort level with their own favorites, sometimes to the point of being unable to achieve a successful implant with leads having other types of fixation, despite a high level of skill.
That partiality also extends to leads having various types of passive fixation. The latter mechanisms also suffer disadvantages, including the fact that leads utilizing them typically are not easily threaded through the vein, and the mechanism tends to be dislodged from the tissue or not be easily seated in place during implantation, as may be expected when one is dealing, by definition, with less positive fixation. Nevertheless, leads with passive fixation devices are much easier to reposition during implantation than are leads with active fixation devices once having engaged and penetrated the tissue. Furthermore, the passive fixation-type leads are typically less complex and therefore easier to manufacture than the active fixation leads.
It is a principal object of the present invention to provide a new and improved passive fixation mechanism for cardiac stimulating or sensing electrodes.
A serious problem with previous approaches to passive fixation of the lead/electrode is that the anchoring means is permanently deployed to contact tissue for seating once the stimulating electrode is positioned to achieve capture. Accordingly, the lead is not easily threaded through the vein. Moreover, some of the tined-types of leads tend to become so enmeshed in the trabeculae that re-positioning of the lead/electrode approaches the order of difficulty encountered with some of the active fixation leads. In this respect, it should be noted that the threshold for a seated lead/electrode may be considerably higher than had been observed just prior to the seating, requiring that the electrode be re-positioned.
Accordingly, it is another object of the present invention to provide an improved passive fixation mechanism for a catheter lead which allows the lead to be inserted easily through the vein for placement of the electrode in proper position in the desired heart chamber, and which further enables the lead to be withdrawn readily or the electrode to be disengaged and repositioned easily to a different location to provide a lower threshold for capture.